Th1, Th2, and Th17 cells are involved in the pathogenesis of DSS-induced colitis.29 A previous study showed that targeted impairment of Th17 cell function could treat CD.30 Besides, transient depletion of Treg cells increased the severity of DSS-induced colitis.31 A previous study demonstrated that B. adolescentis specifically activated Th17 cells, but this effect didn’t induce colon inflammation.32 In our experiment, supplement of B. adolescentis decreased the pro-inflammatory cytokines but increased the anti-inflammatory cytokines of IL-10 and IL-4. The gene discussed is IL4; the disease is Cowden disease.